Gestational diabetes is a common pregnancy complication. Although the precise underlying mechanism has yet to be identified, insulin resistance and inadequate insulin secretion to compensate for it play a central role in the pathophysiology of GDM. Excess adiposity is an important modifiable risk factor for the development of the condition. Mechanisms linking excess adiposity to elevated risk of GDM are not completely understood, but recent evidence points to the crucial role of specific hormones and cytokines (adipokines) secreted by the adipose tissue. The general goal of this project is for research on the pathogenesis of GDM. Under this research theme, the specific aim of this project is to prospectively investigate novel biochemical markers, for instance, biomarkers involved in adipocyte cytokine secretion and metabolism in association with subsequent risk of GDM and fetal overgrowth. This project utilizes bio-specimens from throughout pregnancy from GDM cases and matched controls within the NICHD Fetal Growth Studies. In the past year, we actively worked with the UMN laboratory to obtain data including non-targeted metabolomics data from UC Davis. We are teaming with biostatiticians analyzing the data. Statistical analyses and manuscript preparation on biomarkers of GDM risk are ongoing. The first series of publications have focused on modifiable biomarkers and metabolomics and lipodomic profiling that are functions of major exogenous origin (via dietary intake). In addition, recent analyses examined the insulin-like growth factor (IGF)-axis in early-to-mid pregnancy in relation to subsequent GDM risk. This project identified that dysregulation in the IGF-axis as early as the first trimester in pregnancy may be implicated in the pathogenesis of GDM.